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Ira Tabas

Researcher at Columbia University

Publications -  308
Citations -  53122

Ira Tabas is an academic researcher from Columbia University. The author has contributed to research in topics: Macrophage & Efferocytosis. The author has an hindex of 110, co-authored 293 publications receiving 45403 citations. Previous affiliations of Ira Tabas include Brigham and Women's Hospital & New York University.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
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Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress.

Ira Tabas, +1 more
- 01 Mar 2011 - 
TL;DR: The molecular mechanisms linking ER stress to apoptosis are the topic of this review, with emphases on relevance to pathophysiology and integration and complementation among the various apoptotic pathways induced by ER stress.
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Macrophages in the pathogenesis of atherosclerosis.

Kathryn J. Moore, +1 more
- 29 Apr 2011 - 
TL;DR: The central roles of macrophages in each of the stages of disease pathogenesis are discussed, including atherosclerosis, stroke, and sudden cardiac death.
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The Response-to-Retention Hypothesis of Early Atherogenesis

Kevin Jon Williams, +1 more
- 01 May 1995 - 
TL;DR: Subendothelial retention of atherogenic lipoproteins as the central pathogenic process in atherogenesis is strongly supported, and other contributory processes are either not individually necessary or are not sufficient.